Variation of thyroxine in pregnancy

• Free T4 is a better measure than total T4 in pregnancy due to the increase in thyroid binding globulin.

Some definitions

In parasitology, a definitive host is an organism that harbors a parasite that has reached sexual maturity. An intermediate host is an organism that harbors a parasite that has not yet reached sexual maturity. - Bard

Trypanosomiasis - sleeping sickness

#insect-vector #lymphadenopathy
Pathogen : protozoan - trypanosoma sp.
Vector : Tsetse fly - Glossina
Enedemic to subsaharan africa
About a week after the bite, the patient develops a chancre at the site of the bite.
Other syptoms are lymphadenopathy (painless, posterior chain) and hepatosplenomegaly.
The parasite moves through the lympathic system can can invade the CNS --> late stage symptoms involve CNS dysfunction (aka. sleeping sickness)
Usually a slowly progressing disease; many are diagnosed incidentally.

Treatment: nifurtimox-eflornithine, fexinidazole, pentamidine

Legionella pneumonia

• Legionella pneumophila is a thin, aerobic, pleomorphic, flagellated, non-spore-forming, Gram-negative bacterium of the genus Legionella
• Gram negative, intracellular

• Pneumonia is the commonest manifestation of legionella infection. Infection of other sites is rare.
• Causes bilateral mid to lower zone patchy consolidations.
• Can cause mild to severe disease.
• People get from contaminated air-conditioner water.
  • Person to person transmission doesn't occur.
• Associated features:
  • Hyponatremia
  • Liver enzyme elevation
  • CRP > 100;
  • GI symptoms
  • Exposure (from contaminated water in buildings)
  • Resistance to beta lactams
• Diagnosis: PCR of respiratory secretion but if this is not possible, urinary antigen can be checked.
  • Mnemonic: Comes from (air-conditioning) water and goes in water.
• Mortality can be up to 10%.
• Treatment: fluoquinolone or macrolide.
  • Levofloxacin - inhibits bacterial DNA topoisomerase
  • Azithromycin - 50s ribosomalal subunit and inhibit protein synthesis

Levofloxacin and azithromycin are the preferred agents for the treatment of Legionnaires' disease because these agents are bactericidal, achieve high intracellular concentrations, penetrate lung tissue, and are active against all Legionella species that cause human infection. Alternatives include other fluoroquinolones (eg, moxifloxacin, ciprofloxacin) and other [[Antibiotics#Why clarithromycin? Why is it interchangeable with metronidazole|macrolides]] (eg, clarithromycin, roxithromycin)

[!TIP] Mycoplasma causes immune phenomena

Mycoplasma pneumonia

Mycoplasma is one of the smallest known free living organisms.
No cells wall -> beta lactams won't work.

Commonest manifestation is upper respiratory tract infection.
but mycoplasma pneumonia is a common cause of community acquired pneumonia as well.
Most mycoplasma associated URTI and LRTI are mild and self limiting; They may not even need ABx. Pursuing a microbiological diagnosis usually isn't necessary as management won't change.

Clinically and radiologically, mycoplasma pneumonia has no distinguishing features from other atypical pneumonia except

• Haemolytic anaemia - typically mild and self limiting [[Haematology MCQ discussion#Q 7 Mycoplasma and haemolystic anaemia|Haemolytic Anaemia in mycoplasma infection]]
• presense of upper respiratory symptoms (rhinorhea, ear ache)

CXR - uni / bi lateral reticulonodular patchy opacities. ( Looks almost normal)
Direct Coombs test and cold-agglutinin titers are typically positive

Diagnosis: PCR
?FBC results - WBC mildly elevated

Directed treatment of M. pneumonia − For patients with microbiologically confirmed M. pneumoniae pneumonia, first-line treatment options include macrolides (eg, azithromycin), tetracyclines (eg, doxycycline), and respiratory fluoroquinolones (eg, levofloxacin or moxifloxacin).

Cholera

Agent: Vibrio cholerae - flagellated gram -ve bacteria. (flagella allows it to swim through mucous and reach the epithelium) (O1 and and O139 are the only ones that have caused epidemics)
Symptoms: Infection can be mild but massive "rice water" diarrhoea is the main clinical feature. 50-70% mortality if untreated. Median time to death from symptom onset is a little as 12 hours.

Cholera toxin has A and B subunits. B subunit facillitates toxin entry. A subunit promotes chloride secretion and inhibits sodium chloride resorption ==> Result is profuse water diarrhoea.
Incubation period is around 2 days but can even be hours (Short!)

Stool of patients contains high amounts of Na, K and HCO3.

Diagnosis is by culture of stool on selective media. (peptone alkaline media etc. ) Clinical diagnosis is usually possible.
Complications: Hypo/ hypernatremia, hypokalemia, met. acidosis, hypocalcemia and cramps,
Management : Aggressive fluid replenishment.
Antibiotics shorten disease duration : macrolides, fluoroquinolones and tetracyclines.
Oral killed vaccines and { live attenuated vaccines (for travellers) } is available.
[[2022 May Basic Sciences#Cholera vaccine|Cholera vaccine]]

📑Typhoid

[!INFO] Introduction to salmonella
Salmonellae are motile gram-negative bacilli that infect or colonize a wide range of mammalian hosts.
Salmonellae cause a number of clinical infections in humans; these include:

• Gastroenteritis
• Enteric fever (systemic illness with fever and abdominal symptoms)
• Bacteremia and endovascular infection
• Focal metastatic infections such as osteomyelitis or abscess
• An asymptomatic chronic carrier state
  Salmonella serotypes other than Salmonella typhi and Salmonella paratyphi are collectively known as nontyphoidal salmonellae

#2023GM Q32

📑Enteric fever

[!TIP] Fever + abdominal pain + GI symptoms

Look for specific signs - relative bradycardia, temperature pulse dissociation, rose spots ==> Enteric / Thyphoid fever.

📑Causative agent: Salmonella typhi AND S. Paratyphi A B and S
📑Humans are the only host of these.😔

• Salmonella typhi 👌🏼survive gastric juice and penetrate the small bowel epithelium and disseminate through the lymphoid tissue and blood vessels.
• 📑Epithelium -> Peyer's patches (causing HYPERTROPHY of Peyer's patches) -> RET via lymph and blood -> Eventually, organisms reside 👌🏼within tissue macrophages in the 👌🏼liver, spleen, and bone marrow.
• Necrosis of submucosal tissues -> abdominal pain and possible ileal perforation.

Infection can result in

1. Acute illness
   Symptoms: "stepwise" fever + chills + abdominal pain 📑5-21 days after exposure. (Not rapid like cholera )
   GI symptoms: diarrhoea or constipation + abdominal pain.
   Other signs: relative bradycardia, pulse-temperature dissociation, and "rose spots".
   Rose spots are ❗non tender, blanching papules. - occurs in 2nd week.
   Intestinal rupture (3rd week) -> ? sepsis
   #splenomegaly during 3rd week
   typhoid encephalopathy in severe disease.

2. Chronic carrier state - minority of cases only.

   1. Chronic Salmonella carriage is defined as excretion of the organism in stool or urine >12 months after acute infection
   2. Commoner in females and those with biliary problems like cholelithiasis.

Investigations:

• Include anemia, leukopenia, leukocytosis, and abnormal liver function tests

Diagnosis: Culture of organism from blood, stool, bone marrow, urine or rose spots / ELISA

• Widal test: Detects antibodies but can be positive in endemic areas because of past infection.

Treatment: Antibiotics :

• Fluoroquinolones [[Antibiotics#Ciprofloxacin|Cipfofloxacin]] -> ? resistant -> Ceftriaxone / cefotaxine -> ? resistant -> Meropenem;

Prevention: two types of 📑vaccinations are given : live attenuated (oral) and antigen based (IM)

• To be given to people in high risk areas (jaffna, mullativu, puttalam, nuwara eliya) and high risk occupations (food handler, HCW in contact with tyhpoid patients etc.)

👌🏼Nontyphoidal salmonella

#2019BSQ-OCT/33
(search Non-typhoidal salmonella)

• They cause outbreaks of foodborne gastroenteritis
• Most commonly associated with poultry and eggs.
  • Infants, and those aged > 60 are at higher risk of severe disease.
• Clinical features of nontyhpoidal salmonella gastroenteritis
  • Salmonella gastroenteritis is more severe than usual GE.
  • onset - 8 to 72 hours.
  • Diarrhoea, nausea, vomiting, fever and abdominal cramping.
  • However, usually self limited.
  • Fever resolves in 2-3 days but dirrhoea takes 4 to 10 days.
  • Clinically difficult to differentiate from other types of diarhoea.
  • Diagnosis requires stool culture.
  • Treatment: Antibiotics are usually not required, unless the patient is an infant or old or immunocompromised or has severe disease for some reasons.
    • When indicated, use fluorquinolone for 1 to 2 weeks.
  • Extraintestinal infection
    • Intestinal infection can progress to infect any site. Urinary infection is the commonest. (i.e long bones, visceral etc)
    • Meningitis is rare but occurs in children < 1 year old.
    • Endovascular infection is a serious complication!
      • Commonest site is infrarenal aorta.
    • Treat with ciprofloxacin, levofloxacin or ceftriaxone for 14 days.

Malaria

Comparison of malaria species

Source

[!TIP] Falciparum = F*cked
Infects RBC of all ages, end organ damage and death is common and parasitaemia can be very high!
Worldwide , highest mortality is from Falciparum.

[!TIP] Only organisms containing V in their name have LIVER stages.

P Falciparum => No relapses from liver! FALCIPARUM DOES NOT FORM HYPNOZOITES!

P vivax => relapsing illness, less severe than falciparum. But still can cause end organ damage and death.
P Ovale => Relapsing illness but less severe than vivax
P malariae => Chronic low level parasitaemia and anaemia; resultant chronic anaemia can cause significant morbidity

Malaria red cell entry receptors:

Plasmodium falciparum invades human erythrocytes by redundant pathways.
Unlike P. vivax that has one Duffy Binding-Like (DBL) receptor, P. falciparum has four members of the DBL receptor family.

Malaria life cycle

"sporos" meaning "seed" or "spore," and "zoion" meaning "animal" or "living being."
"merozoite" - "Meros" means "part" or "segment," while "zoion" translates to "animal"
trophē," meaning "nourishment" or "food," and "zoion," meaning "animal"; During the trophozoite stage, the parasite actively feeds on host cells or ingested materials, acquiring the necessary nutrients for growth and reproduction

The life cycles of P. vivax and P. ovale include a dormant hepatic stage called the hypnozoite.
Relapse shows same symptoms as primary infection; can occurs in weeks, months or years
Dormant hypnozoites don't cause symptoms can cannot be detected by any tests

Vivax and ovale infect reticulocytes.

In P Ovale, all stages of the life cycle are seen in the blood film whereas in P. falciparum only trophozoites and gametocytes are seen in the blood. (therefore, if all forms are seen, chloroquine can be given. )

Bone marrow infection:

[!TIP] The two organisms causing the most severe forms of disease infect bone marrow.

• Falciparum has been shown to infect bone marrow, specially in the immature gametocyte stage. Source
• Newer articles state that vivax also infects bone marrow. Source
  Vertical tranmission:
  #2021BSQ-JUL Q08
• All species of malaria can be transmitted in utero.
• Most commonly with Falciparum and vivax.
• Falciparum is well known to cause transplacental transmission. The parasite can be found in intervillous spaces of the placenta.(placental infection) This causes placental inflammation and various placental abnormalities resulting in IUGR, premature delivery, low birth weight.Source

Malaria clinical features

High fevers with delirium

Febrile paroxysms may occur every other day for P. vivax, P. ovale, and P. falciparum and every third day for P.malariae. Paroxysms occurring at regular intervals are more common in the setting of infection due to P. vivax or P. ovale than P. falciparum

Pathogenesis of disease in malaria infection

All species of plasmodium adhere to cell surfaces in humans. In P falciparum, the time of adhesion is a significant portion of the life cycle.

Falciparum infection of RBC -> RBC produces sticky knobs of proteins -> RBC adhere to capillary endothelium -> sequestration -> partial blood flow obstruction -> complications like cerebral malaria and renal failure.

Diagnosis of malaria

Thick and thin films are used for rapid diagnosis. Thick Vs. Thin film preparation

Films should be repeated every 8 - 12 hours if malaria is suspected.

Parasitaemia (usually < 0.1% of red cells are infested)
Severe paracitaemia = > 5% of cells area affected.
Other Lab Ix:
Severe Anemia (massive intravascular haemolysis), thrombocytopenia,
Elevated transaminases,
mild coagulopathy
elevated blood urea nitrogen (BUN) and creatinine

Chronic malaria can cause Hyper-reactive splenomagaly - aka tropical splenomegaly syndrome. Chronic production of IgM -> immune complexes -> stimulation of RET system -> #splenomegaly

Severe Malaria

Severe malaria can occur with any species but patients with severe malaria should be managed as having falciparum.
Severe malaria occurs when there is organ failure; (defined as any one of the following in presence of malaria infection and after excluding other causes)

Many of the clinical findings are the result of the parasitized RBCs adhering to the endothelial cells lining small blood vessels ("cytoadherence") causing small infarcts, capillary leakage, and organ dysfunction

• CNS -> impaired convulsions / seizures
• Metabolic -> ❗Hypoglycaemia is a feature of severe disease / ❗metabolic acidosis
• GIT -> Jaundice.
• Renal -> AKI
• RS -> Pulmonary oedema with desaturation
• Hyperparasitaemia (> 10% in falciparum (or 5% in non immune individuals))

Treatment for severe malaria is IV or IM Artesunate

Blackwater fever is a rare complication of malaria which can be fatal. It is caused by large intravascular haemolysis resulting in haemoglobinuria, anaemia, jaundice and acute kidney injury. Urine is classically black or dark red in colour.The cause of the massive haemolysis is unknown. The treatment is with antimalarials, intravenous fluids and in some cases dialysis. Urinalysis reveals blood which is not seen on microscopy as it is haemoglobinuria.

Treatment of malaria

[!INFO] Summary

• Uncomplicated non falciparum malaria
  • Treatment is directed at the erythrocytic forms.
  • If species unknown of patient develops severe malaria -> treat as for falciparum.
  • If chloroquine sensitive, give chloroquine or ACT.
  • If chloroquine resistant, give ACT.
  • Fever and parasitaemia settle in 2 - 4 days.
  • Antirelapse therapy with primaquine is started when symptoms begin to resolve.
• Treatment of severe malaria:
  • If no ACT resistance, give IV artesunate.
  • If ACT resistance is prevalent (south east asia) -> combine IV quinine with IV ACT.

Falciparum and vivax both have high prevalence of chloloquine resistance!

For falciparum, ACT (artemisinin based combination therapy) is the first line drug.

ACT = artemether + lumefantrine (one of several drug combinations grouped under ACTs). All combinations are equally effective. (If body weight > 65 Kg, artemisinin + lumifantrine may be less effective)

Artemisinins should be administered with a second agent that has a longer half-life than the artemisinin drug to forestall development of artemisinin resistance and to provide an extended duration of drug level to clear parasitemia
Using artemisinins alone would lead to treatment failure.

If ACT is unavailable and if local falciparum is sensitive to chloroquine-> then chloroquine can be used.
Treatment duration is 3 days. Artemisinin resistance is identified if parasite levels are > 100,000 / microL on day 3. If so, treatment duration is extended to 6 days.
South asian P. Vivax is resistant to chloroquine (?sensitive in other regions) -> Give ACT for vivax infections.

Quinine based regiments can be used as alternatives if ACT resistance is prevalent. Consists of quinine + (doxycycline / tetracyclin / clindamycin). ACT is preferred over quinine regiments because quinine regimens can cause reversible tinitus and high tone hearing loss + GI side effects.

Primaquine reduces transmisibility. Main action is to eradicate hyponozoites. Also acts against gametocytes but has no effect against asexual blood stages.
(i.e so it works against hypnozoites and gametocytes)
Primaquine is contraindicated in #pregnancy and children < 6 months old. Primaquine can cause haemolysis in [[Anaemia#G6PD deficiency|G6PD deficiency]].

Mefloquine - given for prophylaxis - can cause acute psychosis if toxicity occurs. Can be used in pregnancy.
Chloroquine and mefloquine are unsuitable as chemoprophylaxis in patients with epilepsy!

Treatment of malaria in #pregnancy

ACT is safe in pregnancy
Chloloquine is safe in pregnancy.
artesunate is safe in any trimester.
Primaquine is problematic because it exacerbates G6PD-deficiency anaemia;

• Therefore, it's contraindicated in pregnancy as the G6PD status of the foetus is unknown.
• Although breast milk concentrations are low, it's not given while the mother is breastfeeding if the infant is found to be G6PD deficient.
• In the above cases, chloroquine is continued until the baby is delivered or until cessation of breast feeding.

Prophylaxis against malaria infection

#2020GM-NOV/Q43

• Mainly important in travellers.
• For falciparum (which is chloroquine resistant in most regions) endemic regions:
  • Atovaquone-proguanil - most expensive one but has less side effects. Taken daily. 2 day before departure and 7 days after return.
  • mefloquine - taken weakly; more convenient for long term travellers. ?to be started one week before departure.
  • Doxycyline - effective against falciparum and other types of malaria. Taken daily and can cause sun sensitization.
  • tafenoquine
  • All high highly effective at preventing malaria.
• Chloroquine can technically be used if the destination has chloroquine senstive falciparum but this is very rare.
• For vivax endemic areas, chloroquine and tafenoquine can be given provided the traveller does not have G6PD deficiency.

Dengue fever

Dengue has an incubation period of about 1 week (3-14 days) so travellers can develop fever about 1 week after returning
flavivirus
Aedes aegypti - day biter
lymphadenopathy can occur. - ?rare

Clinical features of Dengue

A rash (generalized, macular / maculopapular, blanching, pruritic) can occur in the acute phase of dengue as well. (not just the convalescent phase)

Yellow fever

• Viral infection spread by the dengue mosquito.
• occurs in South America and Sub-saharan africa.
• Patient presents with fever and severe flu-like illness.
• Most infections are mild.
• In about 1/5th of patients, the illness initially resolves and then recurts in a so called period of intoxication phase.
• (usual progression is infection, remission, intoxication)
• In the intoxication phase, patient develops
  • AKI, hepatitis with jaundice and bleeding
• It is a WHO notifiable disease.
• Management is supportive.

Hepatitis A

Self limited.
Few progress to fulminant hepatic failure -> poor prognosis.

Measles

Two phases :
Phase 1 : catarrhal phase : rhinorrhoea, cough, conjunctivitis, koplik's spots in the oral mucosa (lasts 2 - 4 days)
Phase 2: Eruptive / exanthematous stage : rash that spreads form the head outward. (fades away in the same order) (occurs 2 - 4 days after onset of fever)
infective 4 days before and 2 days after onset of rash.
Incubation period 8-14 days.
Droplet spread; highly infective.
No foetal abnormalities.
#2021BSQ-NOV/Q37
Subacute sclerosing panencephalitis (symptoms occur due to viral reactivation in teenage years) and post measles encephalomyeltis (2 weeks after infection) are dreaded complications.

Cyclospora cayatensis infection

Protozoan
Obligate human parasite (Humans are only known host)
Ingestion of sporulated oocyst from fruits / vegetables / water -> infection -> infection of GI mucosa
Low grade fever with anorexia, nausea, flatus, diarrhoea (symptoms can be chronic)
Direct faeco oral transmission is not possible as defecated unsporulated oocyst must mature for days / weeks in the environment.
Treatment: trimethoprim sulfamethoxazole.

Schistosoma

[!TIP] Patient goes swimming in fresh water and then presents with haematuria or diarrhoea. NOT A gastrointestinally acquired pathogen.

[!INFO] AKA Bilharziasis
after the name of the disoverer

• Parasitic infection by a trematode (Phylum platyhelminthes)
• Complex life cycle : snails -> intermediate host; human -> definitive host.
• 3 or 4 Species of parasites.
  • S. mansoni and S. japonicum cause intestinal tract disease
  • S. haematobium causes genitourinary tract disease

[!TIP] Mnemonic for the species:

• Haematobium -> haematuria
• Mansoni -> mesenteric veins -> diarrhoea

• After skin penetration the worms migrate to the liver.

  • Then haematobium species lays eggs in the paravesical venous plexus -> eggs migrate to bladder -> haematuria
  • Mansoni and japonicum lay eggs in the mesenteric veins -> eggs migrate to intestinal lumen -> diarrhoea

• Infective stages are excreted via urine and faeces.

• Acute infection : seen in travellers; locals can have low level parasitaemia

  • Acute infection can present with "swimmer's itch" (acute itch after swimming + localized dermatitis - when parasite enters the skin) and/or acute schistosomiasis syndrome (Katayama syndrome), a systemic hypersensitivity reaction to schistosome antigens and circulating immune complexes. (See 'Acute infection' above.)

• Chronic infection - GI - GI ulceration and scarring + blood loss; liver fibrosis and oesophageal varices .

• Diagnosis : urine culture and microscopy,

  • S. haematobium eggs can be demonstrated in urine.
  • Eosinophilia

Treatment: Praziquantel - antihelminthic drug and steroids to reduce inflammation.

Leishmaniasis

#2020BSQ-NOV/Q67
#2020BSQ-JUL/Q41

[!WARNING] Leishmaniasis is a notifiable disease in Sri Lanka as of 2008

Leishmaniasis causes suppurative granulomas

Leishmaniasis in Sri Lanka

[!TIP] Leishmaniasis in Sri Lanka
DCOSL -> Donovani, cutaneous, in Sri Lanka

Source

In SL, leishmaniasis is reported mainly in Anuradphapura, polonnaruwa, hambantota and Matara. The disease was began spreading locally in the 1990s. Incidence has been increasing rapidly in the past decade.

Sri lanka is endemic for Leishmaniasis caused by Leishmania donovani.

In Sri Lanka, Leishmania donovani (usually associated with visceral leshmaniasis (VL)) causes cutaneous leishmaniasis (CL). This is termed dermotropism. However, it can cause VL as well.
Phelbotomus argentipes is the main vector in SL although others are also present.
In SL, Leishmania incidence is seasonal.

Leishmaniasis has a wide spectrum of disease.

Cutaneous leishmaniasis

Protozoan parasite.
Many species; each one having somewhat different clinical picture.

Diffuse cutaneous

Diffuse cutaneous leishmaniasis — is a rare syndrome that occurs mainly in the setting of L.L. aethiopica, L.L. mexicana, and L.L. amazonensis infection.
It begins as a localized lesion that does not ulcerate; rather, amastigotes disseminate to macrophages in other areas of the skin. People who develop DCL usually have a defect in cell mediated immunity.

Musocal leishmaniasis

• AKA espundia.
• Mainly occurs in the 'new world'. (i.e North and south America).
• So the causative parasites are L brazilliensis, guyanensis, panamensis, amazonensis)

Visceral leishmaniasis

aka Kala-azar (Hindi: black fever)

• Leishmania donovani, l. infantum or chagasi; all the others cause cutaneous leishmaniasis.
• Strongly associated with HIV/AIDS
• Main reservoir in Asia is dogs and foxes.
  • 
• Incubation period = 2 months;
• Symptom onset is insidious and patient may feel well despite abnormal clinical findings.
• #hepatosplenomegaly with #lymphadenopathy
• Untreated, the disease will progress to cause pancytopaenia and immunosuppresion leading to death in a year by superadded bacterial infection.
• Diagnosis: Identification of the organisms in aspirate of bone marrow or liver or spleen.
• Associated investigations: pancytopaenia, hypoalbuminaemia, and hypergammaglobulinaemia.
• Treatment: pentavalent antimony salts (Sodium stibogluconate / melumine antimoniate) OR IV amphotericin B and IM paromomycin. Some patients develop post kalar-azar dermal leishmaniasis.

Post kala-azar dermal leishmaniasis (PKDL)

• Associated with Leishmania donovani.
• A chronic skin rash which occurs after treatment of PKDL
• Mimics leprosy in appearance but there is not sensory loss.
• Perioral region is the earliest affected.
• Median time to onset is about 6 months to 2 years after treatment.

Bubonic plague

Yersinia pestis.
Transmitted by bite of rodent associated flea.
Fever, headache, chills, and weakness and one or more swollen, painful lymph nodes (called buboes).
Can be fatal without antibiotics.

Rocky mountain spotted fever

Tick borne disease which can be fatal if untreated.
Ricketsia rickettsii - gram negative obligate intracellular pathogen; infects vascular endothelial cells; causes vasculitis and increased capillary permeability.

• low effective circulating volume -> ADH -> hyponatremia
• Complications - myocarditis, encephalitis, interstitial pneumonitis
  Distributed throughout the Americas.
  Commoner in spring and summer when outdoor activity peaks.
  Non specific symptoms (fever, arthalgia, myalgia) but on 3-5th day of illness, maculopappular rash.
  Serology in the acute phase is unreliable. Prompt treatment must be started on clinical suspicion.

Q fever: Coxiella burnetti

#2020BSQ-JUL/Q54

Zoonosis; Obligate intracellular parasite. commonest reservoir is goats, cattle, cats.
Infective fluids come from anogenital systems : faeces, urine, birth products and milk.
Infection is by inhalation of aerosols. Infectious dose is very small to minimal contact can cause infection.

Pincu is a 2 - 4 weeks.
Infection can cause:

• mild flu like illness
• Pneumonia
• Hepatitis
  Chronic infection manifests as endocarditis, osteomyelitis uveitis and other local infection.
  Cannot culture. Serology is used for diagnosis.
  Treatment is with doxycycline.

Enterococcus infection

#2020GM-NOV/Q14

• Enterococci are commensals in the GI tract.
  • The two main human pathogens are enteroccus faecium and faecalis. Faecalis is more virulent but faecium can be resistant to vancomycin.
• Clinically context: they are associated with nosocomial infections mostly of urinary tract: catheter assocaited UTI, cystitis, pyelonephritis but also infective Endocarditis.
• Treatment is difficult because they are resistant to many antibiotics.
  • They are resistant to penicillin and cephalosporins, macrolides, clindamycin, macrolides and TMP-SMX.
  • However, if sensitive, ampicillin and amoxicillin are the drugs of choice.
  • Vancomycin can be used if they are found to be sensitive.
  • Combination therapy with a cell wall–active agent (eg, ampicillin, vancomycin) and an aminoglycoside (eg, gentamicin, streptomycin) has long been regarded as the standard of care for E faecalis native valve endocarditis.